https://orcid.org/0000-0002-2297-4645
A 57-year-old woman with history of sleep apnoea, hypothyroidism, and remote severe COVID-19 infection presented with a 2-month history of progressive shortness of breath and pedal oedema. Left ventricular (LV) ejection fraction was 25% with severe global hypokinesis but normal wall thickness. Left heart catheterization excluded obstructive coronary artery disease. Cardiac magnetic resonance imaging (CMR) (1.5T Siemens Sola scanner) demonstrated abnormal post-contrast gadolinium kinetics, with difficulty nulling the myocardium relative to blood pool, which can be seen in infiltrative disease such as cardiac amyloidosis. Prominent subendocardial, mid-myocardial, and near-transmural focal late gadolinium enhancement was present within the septum, lateral and inferior walls (Panels A to C). Myocardial native T1 mapping times and extracellular volume (ECV) values were significantly elevated at 1231 ± 106 ms (reference range 950 ± 21 ms) and 51 ± 9% (reference range 26 ± 4%), respectively, supportive of diffusely expanded interstitium (Panel EandH). T2 short tau inversion recovery (STIR) imaging suggested increased papillary muscle signal, but T2 mapping revealed diffusely elevated LV values (60 ± 7 ms; reference range <55 ms) (Panels D and G). Considerations included amyloidosis or myocarditis with diffuse oedema.
Single-photon emission computed tomography/computed tomography (SPECT-CT) Tc-99m-pyrophosphate for transthyretin cardiac amyloidosis (ATTR-CA) was negative. Serum protein electrophoresis revealed an IgG kappa monoclonal gammopathy. She underwent cardiac 18F-fluorodeoxyglucose (FDG)-positron emission tomography (FDG-PET) that revealed a mismatch pattern, with moderate FDG uptake in the basal-mid lateral wall, with a corresponding basal lateral wall perfusion defect (Panels F and I). Given the constellation of findings and absence of extra-cardiac FDG uptake, clinical suspicion shifted towards myocarditis. Cardiac biopsy revealed abundant mononuclear inflammatory cells (lymphocytes and macrophages), consistent with lymphocytic myocarditis. This case illustrates that severe myocarditis may mimic the classic CMR findings of cardiac amyloidosis.
Funding: None declared.
Data availability: The data underlying this article are available in the article.
Author notes
Conflict of interest: None declared.
